Seizures in neurocysticercosis (NCC) occurs as a consequence of inflammation invoked by dying degenerating cysts or are associated by calcified lesions. Two mechanisms likely cause seizures around calcifications. The first type originates from calcifications that show perilesional edema(PE) at the time of a seizure occurrence and the second is associated with calcifications without any changes in the lesion as seen by magnetic resonance imaging (MRI). Studies suggests PE is due to the acute development of inflammation centered around the involved calcification. In endemic populations, a large majority of seizures originate from calcified foci and in a prospective study of an urban population with only calcifications and seizures, 50% of recurrent seizures were associated with perilesional edema. The natural history and prognosis of persons undergoing perilesional edema episodes is unknown. We followed a cohort of patients with documented PE for as long as 30 years and report on the long-term clinical and radiological course of persons undergoing PE episodes. Methods. Twenty-one persons with NCC who experienced >= 1 PE episode were followed for a median of 10.6 years (range, 0.4-29.2 years). Clinical evaluations and magnetic resonance imaging (MRI) were performed at the time of suggestive symptoms and during routine follow-up. PE episodes were documented 78 times, involving 50 of 729 calcifications. Episodes reoccurred in all but 3 persons. The pattern, rate, and number of episodes were variable, commonly chronic, and not significantly associated with time from treatment, number of calcifications, or sex. Seizure was the most common symptom, but almost 30% of episodes were asymptomatic and detected by MRI during routine follow-up. Persons with delayed recurrent episodes were significantly older (age, 42.3 vs 28.8 years; P =.045). Seizures continued to occur in 37.5%, and 2 persons had a severe disabling clinical course. The number and timing of PE episodes in individuals with calcified NCC are variable and commonly chronic, sometimes recurring over decades. A minority of patients developed significant disability. Patients who present with neurocysticercosis (NCC) in the United States are almost always immigrants who have been out of endemic areas for years. As a consequence, they are uncommonly infected with gastrointestinal parasites that cause eosinophilia with the exception of strongyloidiasis. Whether eosinophilia is suggestive of neurocysticercosis (NCC) is controversial and inadequately studied. We determined the presence of eosinophilia (>/= 500 eosinophils/mm3) at clinical presentation in 72 patients with a proven or probable diagnosis of NCC and who had not received corticosteroids within 2 weeks of evaluation and complete blood count. Only two persons whose last possible endemic exposures to NCC were 7 and 6 years earlier had eosinophilia of 500 eosinophils/mm3 and both had a positive antibody serology to strongyloidiasis. In the one subject where a follow-up assessment was possible, the eosinophilia resolved. The likely cause for eosinophilia in both was strongyloidiasis. Therefore, none of the subjects with newly diagnosed NCC had significant eosinophilia. Eosinophilia in newly diagnosed symptomatic NCC subjects who had remote exposure is unusual and should prompt a search for another process or infection. Radiological and inflammatory changes induced by combined treatment with the cysticidal drugs albendazole and praziquantel was studied in naturally infected pigs with neurocysticercosis. Disease manifestations in neurocysticercosis (NCC) are frequently due to inflammation of degenerating Taenia solium brain cysts due either to the natural history of disease or as a result of cysticidal treatment. The pig is the natural intermediate host of t. solium and undergoes a similar pathophysiology response to treatment as human infection and treatment. Acute changes in MRI parameters and inflammation were determine at 0, 2 and 5 days after treatment with praziquantel and albendazole. An increase in inflammation and enhancement ( leakage of gadolinium dye) occurred at 2 days and 5 days after initiation of treatment accompanied by a decrease in cyst size. Cysts with lower cyst volume ratios showed increased post-treatment inflammation, loss of vesicular fluid and cyst wall wrinkling. A significant and drastic reduction of cyst size and increased pericystic enhancement occur in the initial days after antiparasitic treatment as an effect of acute perilesional immune response. These significant changes showed that early anthelmintic efficacy (day two) can be detected using magnetic resonance imaging. Failure to observe early changes could be a sign of treatment failure prompting change in dosing.